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Ameliorative effect of water spinach, Ipomea aquatica (Convolvulaceae), against experimentally induced arsenic toxicity.

Dua TK, Dewanjee S, Gangopadhyay M, Khanra R, Zia-Ul-Haq M, De Feo V - J Transl Med (2015)

Bottom Line: In addition, the serum biochemical and haematological parameters were significantly (p < 0.05-0.01) altered in the NaAsO2-treated animals.However, concurrent administration of AEIA (100 mg/ml) could significantly reinstate the NaAsO2-induced pathogenesis.Presence of substantial quantities of dietary antioxidants within AEIA would be responsible for overall protective effect.

View Article: PubMed Central - PubMed

Affiliation: Advanced Pharmacognosy Research Laboratory, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700032, India. tarunkduaju@gmail.com.

ABSTRACT

Background: Ipomea aquatica (Convolvulaceae) is traditionally used against Arsenic (As) poisoning in folk medicines in India. The present study was designed to explore the therapeutic role of aqueous extract of I. aquatica (AEIA) against As-intoxication.

Methods: AEIA was chemically standardized by spectroscopic and chromatographic analysis. The cytoprotective role of AEIA was measured on isolated murine hepatocytes. The effect on redox status were measured after incubating the hepatocytes with NaAsO2 (10 μM) + AEIA (400 μg/ml). The protective effect of AEIA (400 μg/ml) in expressions of apoptotic proteins were estimated in vitro. The protective role of AEIA was measured by in vivo assay in mice. Haematological, biochemical, As bioaccumulation and histological parameters were evaluated to ensure the protective role of AEIA (100 mg/kg) against NaAsO2 (10 mg/kg) intoxication.

Results: Phytochemical analysis revealed presence of substantial quantities of phenolics, flavonoids, saponins and ascorbic acid in AEIA. Incubation of murine hepatocytes with AEIA (0-400 μg/ml) + NaAsO2 (10 μM) exerted a concentration dependent cytoprotective effect. Incubation of murine hepatocytes with NaAsO2 (10 μM, ~ IC50) induced apoptosis via augmenting oxidative stress. NaAsO2 treated hepatocytes exhibited significantly (p < 0.01) enhanced levels of ROS production, lipid peroxidation and protein carbonylation with concomitant depletion of antioxidant enzymes (p < 0.05-0.01) and GSH (p < 0.01) levels. However, AEIA (400 μg/ml) + NaAsO2 (10 μM) could significantly (p < 0.05-0.01) reinstate the aforementioned parameters to near-normal status. Besides, AEIA (400 μg/ml) could significantly counteract (p <0.05-0.01) ROS mediated alteration in the expressions of apoptotic proteins viz. Bcl-2, BAD, Cyt C, Apaf 1, caspases, Fas and Bid. In in vivo bioassay, NaAsO2 (10 mg/kg) treatment in mice caused significantly (p < 0.05-0.01) elevated As bioaccumulation, ATP levels, DNA fragmentations and oxidative stress in the liver, kidney, heart, brain and testes along with alteration in cytoarchitecture of these organs. In addition, the serum biochemical and haematological parameters were significantly (p < 0.05-0.01) altered in the NaAsO2-treated animals. However, concurrent administration of AEIA (100 mg/ml) could significantly reinstate the NaAsO2-induced pathogenesis.

Conclusion: Presence of substantial quantities of dietary antioxidants within AEIA would be responsible for overall protective effect.

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Related in: MedlinePlus

Effect on antioxidant parameters viz. ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GR, GPx, GST and GSH in absence (NaAsO2) and presence of AEIA (NaAsO2 + AEIA) in experimental mice. Values were expressed as mean ± SE (n = 6). #Values differed significantly from normal control (p < 0.01). $ Values differed significantly from normal control (p < 0.05). *Values differed significantly from NaAsO2 control (p < 0.05). **Values differed significantly from NaAsO2 control (p < 0.01). CAT unit, ‘U’ is defined as μmoles of H2O2 consumed per minute. SOD unit, ‘U’ is defined as the μmoles inhibition of NBT reduction per minute.
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Fig7: Effect on antioxidant parameters viz. ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GR, GPx, GST and GSH in absence (NaAsO2) and presence of AEIA (NaAsO2 + AEIA) in experimental mice. Values were expressed as mean ± SE (n = 6). #Values differed significantly from normal control (p < 0.01). $ Values differed significantly from normal control (p < 0.05). *Values differed significantly from NaAsO2 control (p < 0.05). **Values differed significantly from NaAsO2 control (p < 0.01). CAT unit, ‘U’ is defined as μmoles of H2O2 consumed per minute. SOD unit, ‘U’ is defined as the μmoles inhibition of NBT reduction per minute.

Mentions: The effects of different treatments on redox status within selected organs of experimental mice have been depicted in Figure 7. In this study, As-intoxication significantly enhanced (p < 0.01) intercellular ROS production in liver, kidney, heart, brain and testes of experimental mice. Concurrent treatment of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) prevent the As-mediated ROS generation within the selected tissues. Increased ROS production simultaneously enhanced lipid peroxidation and protein carbonylation. In this study, the extents of lipid peroxidation and protein carbonylation within the tissues of experimental mice were significantly (p < 0.01) increased in NaAsO2 (10 mg/kg) treated mice. However, concurrent treatment of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) reinstate the ROS mediated augmented of lipid peroxidation and protein carbonylation in the tissues of experimental mice. Cellular ubiquinols (co-enzymes Q9 and Q10) participate in cellular electron carriers distributed in intracellular major organelles. In this study, a significant reduction of Q9 (p < 0.05-0.01) and Q10 (p < 0.01) levels in liver, kidney, heart, brain and testes of NaAsO2 (10 mg/kg) treated experimental mice suggested As-induced oxidative stress. However, simultaneous administration of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) prevent As-induced reduction of ubiquinol levels in the selected tissues of experimental mice. Antioxidant enzymes and reduced glutathione (GSH) partake in cellular defense mechanism during oxidative stress. In this study, NaAsO2 (10 mg/kg) intoxication could significantly (p < 0.05-0.01) decrease the levels of antioxidant enzymes and GSH in the selected tissues of experimental mice, when compared with control group. Simultaneous administration of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg), however, could significantly (p < 0.05-0.01) prevent As-induced reduction of antioxidant enzymes and GSH levels to near-normal status in hepatic, renal, cardiac, cerebral and testicular tissues of experimental mice, when compared with NaAsO2 (10 mg/kg) control group.Figure 7


Ameliorative effect of water spinach, Ipomea aquatica (Convolvulaceae), against experimentally induced arsenic toxicity.

Dua TK, Dewanjee S, Gangopadhyay M, Khanra R, Zia-Ul-Haq M, De Feo V - J Transl Med (2015)

Effect on antioxidant parameters viz. ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GR, GPx, GST and GSH in absence (NaAsO2) and presence of AEIA (NaAsO2 + AEIA) in experimental mice. Values were expressed as mean ± SE (n = 6). #Values differed significantly from normal control (p < 0.01). $ Values differed significantly from normal control (p < 0.05). *Values differed significantly from NaAsO2 control (p < 0.05). **Values differed significantly from NaAsO2 control (p < 0.01). CAT unit, ‘U’ is defined as μmoles of H2O2 consumed per minute. SOD unit, ‘U’ is defined as the μmoles inhibition of NBT reduction per minute.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359489&req=5

Fig7: Effect on antioxidant parameters viz. ROS production, lipid peroxidation, protein carbonylation, co-enzyme Q9, co-enzyme Q10, CAT, SOD, GR, GPx, GST and GSH in absence (NaAsO2) and presence of AEIA (NaAsO2 + AEIA) in experimental mice. Values were expressed as mean ± SE (n = 6). #Values differed significantly from normal control (p < 0.01). $ Values differed significantly from normal control (p < 0.05). *Values differed significantly from NaAsO2 control (p < 0.05). **Values differed significantly from NaAsO2 control (p < 0.01). CAT unit, ‘U’ is defined as μmoles of H2O2 consumed per minute. SOD unit, ‘U’ is defined as the μmoles inhibition of NBT reduction per minute.
Mentions: The effects of different treatments on redox status within selected organs of experimental mice have been depicted in Figure 7. In this study, As-intoxication significantly enhanced (p < 0.01) intercellular ROS production in liver, kidney, heart, brain and testes of experimental mice. Concurrent treatment of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) prevent the As-mediated ROS generation within the selected tissues. Increased ROS production simultaneously enhanced lipid peroxidation and protein carbonylation. In this study, the extents of lipid peroxidation and protein carbonylation within the tissues of experimental mice were significantly (p < 0.01) increased in NaAsO2 (10 mg/kg) treated mice. However, concurrent treatment of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) reinstate the ROS mediated augmented of lipid peroxidation and protein carbonylation in the tissues of experimental mice. Cellular ubiquinols (co-enzymes Q9 and Q10) participate in cellular electron carriers distributed in intracellular major organelles. In this study, a significant reduction of Q9 (p < 0.05-0.01) and Q10 (p < 0.01) levels in liver, kidney, heart, brain and testes of NaAsO2 (10 mg/kg) treated experimental mice suggested As-induced oxidative stress. However, simultaneous administration of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg) could significantly (p < 0.05-0.01) prevent As-induced reduction of ubiquinol levels in the selected tissues of experimental mice. Antioxidant enzymes and reduced glutathione (GSH) partake in cellular defense mechanism during oxidative stress. In this study, NaAsO2 (10 mg/kg) intoxication could significantly (p < 0.05-0.01) decrease the levels of antioxidant enzymes and GSH in the selected tissues of experimental mice, when compared with control group. Simultaneous administration of AEIA (100 mg/kg) along with NaAsO2 (10 mg/kg), however, could significantly (p < 0.05-0.01) prevent As-induced reduction of antioxidant enzymes and GSH levels to near-normal status in hepatic, renal, cardiac, cerebral and testicular tissues of experimental mice, when compared with NaAsO2 (10 mg/kg) control group.Figure 7

Bottom Line: In addition, the serum biochemical and haematological parameters were significantly (p < 0.05-0.01) altered in the NaAsO2-treated animals.However, concurrent administration of AEIA (100 mg/ml) could significantly reinstate the NaAsO2-induced pathogenesis.Presence of substantial quantities of dietary antioxidants within AEIA would be responsible for overall protective effect.

View Article: PubMed Central - PubMed

Affiliation: Advanced Pharmacognosy Research Laboratory, Department of Pharmaceutical Technology, Jadavpur University, Kolkata, 700032, India. tarunkduaju@gmail.com.

ABSTRACT

Background: Ipomea aquatica (Convolvulaceae) is traditionally used against Arsenic (As) poisoning in folk medicines in India. The present study was designed to explore the therapeutic role of aqueous extract of I. aquatica (AEIA) against As-intoxication.

Methods: AEIA was chemically standardized by spectroscopic and chromatographic analysis. The cytoprotective role of AEIA was measured on isolated murine hepatocytes. The effect on redox status were measured after incubating the hepatocytes with NaAsO2 (10 μM) + AEIA (400 μg/ml). The protective effect of AEIA (400 μg/ml) in expressions of apoptotic proteins were estimated in vitro. The protective role of AEIA was measured by in vivo assay in mice. Haematological, biochemical, As bioaccumulation and histological parameters were evaluated to ensure the protective role of AEIA (100 mg/kg) against NaAsO2 (10 mg/kg) intoxication.

Results: Phytochemical analysis revealed presence of substantial quantities of phenolics, flavonoids, saponins and ascorbic acid in AEIA. Incubation of murine hepatocytes with AEIA (0-400 μg/ml) + NaAsO2 (10 μM) exerted a concentration dependent cytoprotective effect. Incubation of murine hepatocytes with NaAsO2 (10 μM, ~ IC50) induced apoptosis via augmenting oxidative stress. NaAsO2 treated hepatocytes exhibited significantly (p < 0.01) enhanced levels of ROS production, lipid peroxidation and protein carbonylation with concomitant depletion of antioxidant enzymes (p < 0.05-0.01) and GSH (p < 0.01) levels. However, AEIA (400 μg/ml) + NaAsO2 (10 μM) could significantly (p < 0.05-0.01) reinstate the aforementioned parameters to near-normal status. Besides, AEIA (400 μg/ml) could significantly counteract (p <0.05-0.01) ROS mediated alteration in the expressions of apoptotic proteins viz. Bcl-2, BAD, Cyt C, Apaf 1, caspases, Fas and Bid. In in vivo bioassay, NaAsO2 (10 mg/kg) treatment in mice caused significantly (p < 0.05-0.01) elevated As bioaccumulation, ATP levels, DNA fragmentations and oxidative stress in the liver, kidney, heart, brain and testes along with alteration in cytoarchitecture of these organs. In addition, the serum biochemical and haematological parameters were significantly (p < 0.05-0.01) altered in the NaAsO2-treated animals. However, concurrent administration of AEIA (100 mg/ml) could significantly reinstate the NaAsO2-induced pathogenesis.

Conclusion: Presence of substantial quantities of dietary antioxidants within AEIA would be responsible for overall protective effect.

Show MeSH
Related in: MedlinePlus